Demonstration of a universal one-way quantum quadratic phase gate

We demonstrate a quadratic phase gate for one-way quantum computation in the continuous-variable regime. This canonical gate, together with phase-space displacements and Fourier rotations, completes the set of universal gates for realizing any single-mode Gaussian transformation such as arbitrary squeezing. As opposed to previous implementations of measurement-based squeezers, the current gate is fully controlled by the local oscillator phase of the homodyne detector. Verifying this controllability, we give an experimental demonstration of the principles of one-way quantum computation over continuous variables. Moreover, we can observe sub-shot-noise quadrature variances in the output states, confirming that nonclassical states are created through cluster computation.Comment: 5 pages, 4 figure

Parallel generation of quadripartite cluster entanglement in the optical frequency comb

Scalability and coherence are two essential requirements for the experimental implementation of quantum information and quantum computing. Here, we report a breakthrough toward scalability: the simultaneous generation of a record 15 quadripartite entangled cluster states over 60 consecutive cavity modes (Qmodes), in the optical frequency comb of a single optical parametric oscillator. The amount of observed entanglement was constant over the 60 Qmodes, thereby proving the intrnisic scalability of this system. The number of observable Qmodes was restricted by technical limitations, and we conservatively estimate the actual number of similar clusters to be at least three times larger. This result paves the way to the realization of large entangled states for scalable quantum information and quantum computing.Comment: 4 pages + 7 supplemental-info pages, 6+1 figures, accepted by Physical Review Letters. One minor revision to main text. One error corrected in Eq. (18) of Supplemental informatio

Demonstration of a quantum nondemolition sum gate

The sum gate is the canonical two-mode gate for universal quantum computation based on continuous quantum variables. It represents the natural analogue to a qubit C-NOT gate. In addition, the continuous-variable gate describes a quantum nondemolition (QND) interaction between the quadrature components of two light fields. We experimentally demonstrate a QND sum gate, employing the scheme by R. Filip, P. Marek, and U.L. Andersen [\pra {\bf 71}, 042308 (2005)], solely based on offline squeezed states, homodyne measurements, and feedforward. The results are verified by simultaneously satisfying the criteria for QND measurements in both conjugate quadratures.Comment: 4 pages, 4 figure

A Role of Intestinal Alkaline Phosphatase 3 (Akp3) in Inorganic Phosphate Homeostasis

Background/Aims: Hyperphosphatemia is a serious complication of late-stage chronic kidney disease (CKD). Intestinal inorganic phosphate (Pi) handling plays an important role in Pi homeostasis in CKD. We investigated whether intestinal alkaline phosphatase 3 (Akp3), the enzyme that hydrolyzes dietary Pi compounds, is a target for the treatment of hyperphosphatemia in CKD. Methods: We investigated Pi homeostasis in Akp3 knockout mice (Akp3-/-). We also studied the progression of renal failure in an Akp3-/- mouse adenine treated renal failure model. Plasma, fecal, and urinary Pi and Ca concentration were measured with commercially available kit, and plasma fibroblast growth factor 23, parathyroid hormone, and 1,25(OH)2D3 concentration were measured with ELISA. Brush border membrane vesicles were prepared from mouse intestine using the Ca2+ precipitation method and used for Pi transport activity and alkaline phosphatase activity. In vivo intestinal Pi absorption was measured with oral 32P administration. Results: Akp3-/- mice exhibited reduced intestinal type II sodium-dependent Pi transporter (Npt2b) protein levels and Na-dependent Pi co-transport activity. In addition, plasma active vitamin D levels were significantly increased in Akp3-/- mice compared with wild-type animals. In the adenine-induced renal failure model, Akp3 gene deletion suppressed hyperphosphatemia. Conclusion: The present findings indicate that intestinal Akp3 deletion affects Na+-dependent Pi transport in the small intestine. In the adenine-induced renal failure model, Akp3 is predicted to be a factor contributing to suppression of the plasma Pi concentration

小腸のリン恒常性における小腸型アルカリホスファターゼ(Akp3)の役割について

Background/Aims: Hyperphosphatemia is a serious complication of late-stage chronic kidney disease (CKD). Intestinal inorganic phosphate (Pi) handling plays an important role in Pi homeostasis in CKD. We investigated whether intestinal alkaline phosphatase 3 (Akp3), the enzyme that hydrolyzes dietary Pi compounds, is a target for the treatment of hyperphosphatemia in CKD. Methods: We investigated Pi homeostasis in Akp3 knockout mice (Akp3-/-). We also studied the progression of renal failure in an Akp3-/- mouse adenine treated renal failure model. Plasma, fecal, and urinary Pi and Ca concentration were measured with commercially available kit, and plasma fibroblast growth factor 23, parathyroid hormone, and 1,25(OH)2D3 concentration were measured with ELISA. Brush border membrane vesicles were prepared from mouse intestine using the Ca2+ precipitation method and used for Pi transport activity and alkaline phosphatase activity. In vivo intestinal Pi absorption was measured with oral 32P administration. Results: Akp3-/- mice exhibited reduced intestinal type II sodium-dependent Pi transporter (Npt2b) protein levels and Na-dependent Pi co-transport activity. In addition, plasma active vitamin D levels were significantly increased in Akp3-/- mice compared with wild-type animals. In the adenine-induced renal failure model, Akp3 gene deletion suppressed hyperphosphatemia. Conclusion: The present findings indicate that intestinal Akp3 deletion affects Na+-dependent Pi transport in the small intestine. In the adenine-induced renal failure model, Akp3 is predicted to be a factor contributing to suppression of the plasma Pi concentration

Diffusion tensor imaging of brain abnormalities induced by prenatal exposure to radiation in rodents.

We assessed brain abnormalities in rats exposed prenatally to radiation (X-rays) using magnetic resonance imaging (MRI) and histological experiments. Pregnant rats were divided into 4 groups: the control group (n = 3) and 3 groups that were exposed to different radiation doses (0.5, 1.0, or 1.5 Gy; n = 3 each). Brain abnormalities were assessed in 32 neonatal male rats (8 per group). Ex vivo T2-weighted imaging and diffusion tensor imaging (DTI) were performed using 11.7-T MRI. The expression of markers of myelin production (Kluver-Barrera staining, KB), nonpyramidal cells (calbindin-D28k staining, CaBP), and pyramidal cells (staining of the nonphosphorylated heavy-chain neurofilament SMI-32) were histologically evaluated. Decreased brain volume, increased ventricle volume, and thinner cortices were observed by MRI in irradiated rats. However, no abnormalities in the cortical 6-layered structure were observed via KB staining in radiation-exposed rats. The DTI color-coded map revealed a dose-dependent reduction in the anisotropic signal (vertical direction), which did not represent reduced numbers of pyramidal cells; rather, it indicated a signal reduction relative to the vertical direction because of low nerve cell density in the entire cortex. We conclude that DTI and histological experiments are useful tools for assessing cortical and hippocampal abnormalities after prenatal exposure to radiation in rats